Cardiopatía chagásica en pacientes de área endémica versus contagiados en forma ocasional

Abstract

DescriptoresEnfermedad de Chagas, epidemiologia. Cardiopatias, diagnostico. Formas de contagio. Cardiopatía chagásica. ResumenEl objetivo del trabajo fue comparar el grado de compromiso cardíaco entre dos poblaciones de chagásicos, con residencia permanente en área endémica y con exposición ocasional al parásito y con contagio por vía no vectorial (transfusional, connatal, y otras). Los resultados mostraron que los infectados ocasionales presentan menor presencia de cardiopatía; y cuando presentan cardiopatía, tienen menor prevalencia de miocardiopatía dilatada que los infectados con residencia permanente en el área endémica. También se plantea el rol del parásito, la cantidad de infecciones, los mecanismos inmuno-patogénicos desarrollados, la calidad de vida y el tipo de tareas laborales en la diferente evolución de estos pacientes. AbstractThe aim of the study was to compare the degree of cardiac compromise between two patient groups infected with Chagas' disease, A) those permanently residing in endemic areas and B) those sporadically exposed to the parasite and indirectly (non-vector) infected (transfusion , mother-to-child transmission, etc. INTRODUCCIÓNLa población que vive expuesta al riesgo de contraer la enfermedad de Chagas en zonas endémicas de América Latina es de aproximadamente 90 millones de personas, de las cuales se estima que, al menos 18 millones ya están infectadas por el Trypanosoma cruzi. En Argentina, para una población estimada en el año 1997 de 35 millones de habitantes, se calculaba en siete millones la población en riesgo de contraer la infección, con una prevalencia del 7,5%, es decir, 2.640.000 individuos con serología reactiva para Chagas. 5 Los estudios de seguimiento longitudinal demuestran que entre el 70% y el 80% de los pacientes chagásicos permanecen durante toda su vida en la forma indeterminada, asintomáticos y sin lesiones aparentes, sólo con la serología positiva. Entre el 20% y 30% restante evolucionan hacia el daño crónico, donde aproximadamente una tercera parte de ellos presenta complicaciones dado lo avanzado de las

Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial

“…Additional evidence to support this concept has been found in other studies in animal models of T. cruzi infection and in humans with Chagas disease: (1) tissue parasite load clearly correlates with the intensity of inflammation in animal models of T. cruzi infection ( Zhang & Tarleton 1999 ); (2) reinfection or continued exposure to infection by permanently residing in areas of active transmission leads to an increase of both the parasite load and disease severity in animal models and in infected humans ( Bustamante et al 2002 , Storino et al 2002) ; (3) trypanocidal treatment with benznidazole, nifurtimox, or fexinidazole does not eradicate the parasite, but the reduced parasite burden does attenuate the myocarditis in animal models ( Andrade et al 1991 , Garcia et al 2005 , Bahia et al 2012) ; (4) T. cruzi genetic material has been consistently detected in cardiac specimens from patients with chronic Chagas cardiomyopathy, but not in cardiac specimens from seropositive patients who died without clinical signs of cardiac disease ( Jones et al 1992) ; 5) T. cruzi DNA was detectable by PCR methods in the peripheral blood of 86% of patients with well-defined chronic Chagas cardiomyopathy ( Salomone et al 2000) .…”

Congenital and oral transmission of American trypanosomiasis: an overview of physiopathogenic aspects

“…In studies performed by Storino et al . (2002), congenitally infected patients presented lower prevalence of cardiac alterations in comparison with patients infected by the vectorial route as well as a lower prevalence of cardiac eccentric hypertrophy (Bittencourt, 1963; Atias et al 1985; Azogue et al 1985; Storino et al 2002;Torrico et al 2004; Carlier, 2005; Schijman, 2006; Punukollu et al 2007).…”

Epidemiological modeling of Trypanosoma cruzi: Low stercorarian transmission and failure of host adaptive immunity explain the frequency of mixed infections in humans

“…[57], [58]), but we also expect individuals will face multiple reinfections as the immune response mounted during primary infection is likely not to be fully protective [59]. While such reinfections are thought to have important effects on cardiomyopathy [28, 29, 32] and the probability of congenital transmission [60], little is known about their frequency in rural communities. To determine the amount of reinfections per individual thus remains a key challenge to improve our understanding of the disease dynamics and its impact on the populations.…”

“…It has been repeatedly proposed that infected people living in endemic areas suffer from frequent reinfections, and that such reinfections increase the strength of cardiomyopathy in humans [28, 29, 32], just as they do in mice [20–22, 30, 31]. Although those epidemiological studies were based on sound statistical comparisons between individuals with different levels of exposure to vectors, none of them provided estimates of the actual level of vector-human contacts and its associated number of reinfection events per person.…”

“…Several authors proposed a role of reinfections in pathogeny. Although parasitaemia is lower in the reinfections compared to the primary infection in animal models [20, 22, 23], reinfections may aggravate chronic disease in mice [20–22, 30, 31] and they may be associated to chronic cardiac damage in humans [28, 29, 32]. To determine the frequency of reinfections and the ability of the human immune system to prevent them is thus essential to our understanding of the disease dynamics.…”